Castrillon D H, Gönczy P, Alexander S, Rawson R, Eberhart C G, Viswanathan S, DiNardo S, Wasserman S A
Department of Biochemistry, University of Texas Southwestern Medical Center, Dallas 75235-9038.
Genetics. 1993 Oct;135(2):489-505. doi: 10.1093/genetics/135.2.489.
We describe 83 recessive autosomal male-sterile mutations, generated by single P element mutagenesis in Drosophila melanogaster. Each mutation has been localized to a lettered subdivision of the polytene map. Reversion analyses, as well as complementation tests using available chromosomal deficiencies, indicate that the insertions are responsible for the mutant phenotypes. These mutations represent 63 complementation groups, 58 of which are required for spermatogenesis. Phenotypes of the spermatogenesis mutants were analyzed by light microscopy. Mutations in 12 loci affect germline proliferation, spermatocyte growth, or meiosis. Mutations in 46 other loci disrupt differentiation and maturation of spermatids into motile sperm. This collection of male-sterile mutants provides the basis for a molecular genetic analysis of spermatogenesis.
我们描述了通过在黑腹果蝇中进行单P因子诱变产生的83个隐性常染色体雄性不育突变。每个突变已定位到多线染色体图谱的一个字母分区。回复分析以及使用现有染色体缺失进行的互补测试表明，插入导致了突变表型。这些突变代表63个互补群，其中58个是精子发生所必需的。通过光学显微镜分析了精子发生突变体的表型。12个位点的突变影响生殖系增殖、精母细胞生长或减数分裂。其他46个位点的突变破坏了精子细胞分化和成熟为活动精子的过程。这个雄性不育突变体集合为精子发生的分子遗传分析提供了基础。
